Species | Target name | Source | Bibliographic reference |
---|---|---|---|
Homo sapiens | progesterone receptor | Starlite/ChEMBL | References |
Homo sapiens | androgen receptor | Starlite/ChEMBL | References |
Homo sapiens | nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor) | Starlite/ChEMBL | References |
Homo sapiens | nuclear receptor subfamily 3, group C, member 2 | Starlite/ChEMBL | References |
Activity type | Activity value | Assay description | Source | Reference |
---|---|---|---|---|
EC50 (functional) | = 7.1 nM | Agonist activity at glucocorticoid receptor in human HepG2 cells co-transfected with GRE assessed as transactivation activity by luciferase reporter gene assay | ChEMBL. | 21115247 |
EC50 (functional) | = 7.1 nM | Agonist activity at GR expressed in african green monkey CV1 cells transfected with luciferase gene linked to MMTV promoter assessed as induction of luciferase transactivation activity relative to Dexamethasone | ChEMBL. | 21316964 |
Efficacy (functional) | = 81 % | Agonist activity at human GR expressed in NHDF cells assessed as inhibition of IL-6 production by ELISA | ChEMBL. | 21316964 |
Efficacy (functional) | = 95 % | Agonist activity at GR expressed in IL-1beta- and TNFalpha-stimulated HepG2 cells assessed as inhibition of NFKB- or AP-1 mediated E-selectin transcription by luciferase reporter gene assay | ChEMBL. | 21316964 |
Efficacy (binding) | = 96 % | Transrepression activity at glucocorticoid receptor in IL-1beta-stimulated human HepG2 cells assessed as inhibition of AP1 response element-induced IL-6 production by ELISA relative to Dexamethasone | ChEMBL. | 21115247 |
Efficacy (binding) | = 101 % | Transrepression activity at glucocorticoid receptor in TNFalpha/IL1beta-stimulated human HepG2 cells assessed as inhibition of NFkappaB-dependent E-selectin transcription by luciferase reporter gene assay relative to Dexamethasone | ChEMBL. | 21115247 |
Efficacy (functional) | = 144 % | Agonist activity at glucocorticoid receptor in human HepG2 cells co-transfected with GRE assessed as transactivation activity by luciferase reporter gene assay relative to Dexamethasone | ChEMBL. | 21115247 |
Efficacy (functional) | = 144 % | Agonist activity at GR expressed in african green monkey CV1 cells transfected with luciferase gene linked to MMTV promoter assessed as induction of luciferase transactivation activity | ChEMBL. | 21316964 |
IC50 (binding) | = 1.1 nM | Transrepression activity at glucocorticoid receptor in TNFalpha/IL1beta-stimulated human HepG2 cells assessed as inhibition of NFkappaB-dependent E-selectin transcription by luciferase reporter gene assay | ChEMBL. | 21115247 |
IC50 (functional) | = 1.1 nM | Agonist activity at GR expressed in IL-1beta- and TNFalpha-stimulated HepG2 cells assessed as inhibition of NFKB- or AP-1 mediated E-selectin transcription by luciferase reporter gene assay relative to Dexamethasone | ChEMBL. | 21316964 |
IC50 (functional) | = 7.8 nM | Agonist activity at human GR expressed in NHDF cells assessed as inhibition of IL-6 production by ELISA relative to Dexamethasone | ChEMBL. | 21316964 |
IC50 (binding) | = 16 nM | Transrepression activity at glucocorticoid receptor in IL-1beta-stimulated human HepG2 cells assessed as inhibition of AP1 response element-induced IL-6 production by ELISA | ChEMBL. | 21115247 |
Ki (binding) | = 1.7 nM | Displacement of radiolabeled Dexamethasone from glucocorticoid receptor expressed in baculovirus | ChEMBL. | 21115247 |
Ki (binding) | = 1.7 nM | Displacement of radiolabeled Dexamethasone from GR | ChEMBL. | 21316964 |
Ki (binding) | = 800 nM | Binding affinity to mineralocorticoid receptor | ChEMBL. | 21115247 |
Ki (binding) | = 900 nM | Binding affinity to androgen receptor | ChEMBL. | 21115247 |
Ki (binding) | = 1200 nM | Binding affinity to progesterone receptor | ChEMBL. | 21115247 |
Many chemical entities in TDR Targets come from high-throughput screenings with whole cells or tissue samples, and not all assayed compounds have been tested against a single a single target protein, probably because they get ruled out during screening process. Even if these compounds may have not been of interest in the original screening, they may come as interesting leads for other screening assays. Furthermore, we may be able to propose drug-target associations using chemical similarities and network patterns.
2 literature references were collected for this gene.